ArticleInfection and immunity1999
Gamma interferon stimulates rat alveolar macrophages to kill Pneumocystis carinii by L-arginine- and tumor necrosis factor-dependent mechanisms.
Article in Infection and immunity, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 43 citations in OpenAlex.
- Immune Responses toJournal of inflammation research · 2026Review
- Immune responses of different hosts toEuropean respiratory review : an official journal of the European Respiratory Society · 2025Review
- T-cell subsets inClinical & translational immunology · 2025Review
- Nitric oxide for the prevention and treatment of viral, bacterial, protozoal and fungal infections.F1000Research · 2021Review
- Proinflammatory Effects of Respiratory Syncytial Virus-Induced Epithelial HMGB1 on Human Innate Immune Cell Activation.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Mechanisms of Action of Vitamin D as Supplemental Therapy for Pneumocystis Pneumonia.Antimicrobial agents and chemotherapy · 2017Article
- Differential Macrophage Polarization from Pneumocystis in Immunocompetent and Immunosuppressed Hosts: Potential Adjunctive Therapy during Pneumonia.Infection and immunity · 2017Article
- B cell production of tumor necrosis factor in response to Pneumocystis murina infection in mice.Infection and immunity · 2013Article
- Ethanol (EtOH)-induced TGF-β1 and reactive oxygen species production are necessary for EtOH-induced alveolar macrophage dysfunction and induction of alternative activation.Alcoholism, clinical and experimental research · 2012Article
- Colonization by Pneumocystis jirovecii and its role in disease.Clinical microbiology reviews · 2012Review
- Defective nitric oxide production by alveolar macrophages during Pneumocystis pneumonia.American journal of respiratory cell and molecular biology · 2011Article
- Current understanding of Pneumocystis immunology.Future microbiology · 2010Review
- Decreased inflammatory response in Toll-like receptor 2 knockout mice is associated with exacerbated Pneumocystis pneumonia.Microbes and infection · 2008Article
- Contribution of T cell subsets to the pathophysiology of Pneumocystis-related immunorestitution disease.American journal of physiology. Lung cellular and molecular physiology · 2006Article
- Alveolar macrophage-mediated killing of Pneumocystis carinii f. sp. muris involves molecular recognition by the Dectin-1 beta-glucan receptor.The Journal of experimental medicine · 2003Article
- Genetically engineered macrophages expressing IFN-gamma restore alveolar immune function in scid mice.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Pneumocystis carinii pneumonia remains a serious complication for immunocompromised patients. In the present study, P. carinii organisms interacted with gamma interferon (IFN-gamma)-stimulated alveolar macrophages (AMs) to activate the L-arginine-dependent cytocidal pathway involving reactive nitrogen intermediates (RNI) that were assayed as nitrite (NO2-). Unstimulated cultures of AMs produced negligible quantities of RNI. Addition of P. carinii organisms to IFN-gamma-primed AMs resulted in greatly enhanced production of RNI. NO2- levels increased from 0.8 +/- 0.4 to 11.1 +/- 3.8 microM as early as 6 h after P. carinii organisms were incubated with IFN-gamma-stimulated AMs and to 35.1 +/- 8.9 microM after a 24-h incubation, a near-maximum level. High levels of NO2- were produced by AMs primed with as little as 10 U of IFN-gamma per ml in the presence of P. carinii, and a 20-fold increase in IFN-gamma concentration resulted in only a further 65% increase in NO2- production. RNI-dependent killing of P. carinii was demonstrated by both a 51Cr release assay and a [35S]methionine pulse immunoprecipitation assay. Addition of either monoclonal tumor necrosis factor alpha (TNF-alpha) neutralizing antibody or 200 microM NG-monomethyl-L-arginine (L-NGMMA), a competitive inhibitor of the L-arginine-dependent pathway, significantly decreased NO2- production and reduced P. carinii killing. TNF-alpha alone had no effect on P. carinii viability. These results suggest that (i) the specific interaction of P. carinii organisms with IFN-gamma-primed AMs triggers the production of RNI, (ii) RNI are toxic to P. carinii, and (iii) TNF-alpha likely plays a central role in mediating P. carinii killing by IFN-gamma-stimulated AMs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.